To probe the mechanism of the sex differential in lipoprotein metabolism (and in turn the sex differential in atheroslcerosis and indeed longevity itself in Occidental societies), exogegnous progestin or estrogen will be administered to normolipidemic post-menopausal women. The effects of a non-androgenic progestin (medroxyprogesterone) will be contrasted with those of an androgenic 19-nortestosterone derivative (norgestrel), a primarily premenopausal estrogen (17Beta-estradiol), and a post-menopausal estrogen (estrone). Paired studies of plasma lipids, lipoproteins (VLDL, IDL, LDL, HDL2, HDL3), apolipoproteins (B, A-I, A-II, E) post-heparin plasma hepatic triglyceride lipase (HTGL) and lipoprotein lipase (LPL), will be performed before and during 3 graduated doses of the progestin or estrogen. Subjects will be given a metabolic isocaloric diet of 40% F, 45% CHO, 15% P, P/S 0.8, cholesterol 450 mg/d throughout the study. Radio-iodinated apolipoprotein turnover (VLDL apoB, and apoA-I) will be performed before administration of the progestin or estrogen and during the high dose of the steroid. Multicompartmental mathematical modelling will be performed to analyze the regulation of lipoprotein metabolism in the basal state and its modulation by the progestin and estrogen using the results of the steady state tracer studies to constrain modelling of the non-steady state unlabelled lipid, lipoprotein, apoprotein, and post-heparin plasma triglyceride lipase data.